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onsdag den 6. marts 2013

Mitochondrial dysfunction - influence on TRPA1

In my last blogposts I have brought links to many articles informing that the ion channel Transient Receptor Potential Ankyrin 1 (TRPA1) is affected in a number of diseases/conditions, which has relation to Myalgisk encephalomyeltitis (ME). This is Multiple Chemical Sensitivity (MCS), inflammation, pain (fibromyalgia), autonomic dysfunction, Irritable Bowel Syndrome (IBS), bladder pain syndrome and neuropathy.

TRPA1 and the ion channel Transient Receptor Potential Vanilloid 1 (TRPV1) are also involved in a condition called exercise-induced anaphylaxis. And something is wrong about exercise and ME. Is there a shared biochemistry?

Thus, it is reasonable to suspect TRPA1 is affected in ME.

For many years researchers have looked at the relationship between ME and mitochondrial dysfunction. It is an obvious idea to see how TRPA1 and TRPV1are affected by mitochondrial dysfunction.

There is growing evidence that the mitochondrial dysfunction contributes to the complex mechanism of many diseases. Increased formation of Reactive Oxygen Species (ROS) are suspected to contribute to the chronic inflammatory condition in many diseases such as Type II diabetes, cardiovascular disease, and neuroinflammation. And we already know ROS are elevated in ME.

Mitochondrias and TRPA1 are found in peripheral terminals of sensory nerves. A group of researchers wanted to investigate how ROS from mitochondrial dysfunction could affect TRPA1 (and TRPV1). For this experiment they used "bronchopulmonary C fibers" (the nerve fiber, which is connected to the lungs) from mice.

The experimental description can be read by the article mentioned below. I am just quoting the exciting conclusion:" In conclusion, we present evidence that acute mitochondrial dysfunction activates airway sensory nerves preferentially via TRPA1 through the actions of mitochondrially-derived ROS. This represents a novel mechanism by which inflammation may be transduced into nociceptive electrical signaling."

Now, we know that TRPA1 and mitochondrial dysfunction are linked together. Can we use this knowledge in the research into ME and co-morbid conditions?